Lopid is an effective medication which helps to fight with high levels of serum triglycerides. Lopid acts by reducing the production of triglycerides in the liver. It is fibrates.
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Also known as: Gemfibrozil.
Lopid target is to fight against high levels of serum triglycerides.
Lopid acts by reducing the production of triglycerides in the liver. It is fibrates.
Generic name of Lopid is Gemfibrozil.
Brand name of Lopid is Lopid.
Take Lopid tablets orally.
Take Lopid twice a day with water at the same time.
Do not crush or chew it.
If you want to achieve most effective results do not stop taking Lopid suddenly.
If you overdose Lopid and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Lopid overdosage: arthralgia, muscle pain, vomiting, abdominal cramps, diarrhea, nausea.
Store at room temperature between 20 and 25 degrees C (68 and 77 degrees F) away from moisture and heat. Protect from light and humidity. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Lopid are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Lopid if you are allergic to Lopid components.
Do not take Lopid if you're pregnant or you plan to have a baby, or you are a nursing mother.
Do not use potassium supplements or salt substitutes.
Be careful with Lopid if you are taking cholesterol-lowering medications (statins) such as atorvastatin (Lipitor), fluvastatin (Lescol), lovastatin (Mevacor), pravastatin (Pravachol), and simvastatin (Zocor); and repaglinide (Prandin), anticoagulants ('blood thinners') such as warfarin (Coumadin).
Be careful with Lopid if you suffer from or have a history of kidney, liver, gallbladder disease.
Do not stop taking Lopid suddenly.
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Although myopathy is considered an adverse effect of treatment with 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors and fibrates in combined hyperlipidemia, the present study was performed to investigate whether combined hyperlipidemia itself is associated with skeletal muscle pathology and whether lipid-lowering intervention has beneficial effects. To investigate whether combined hyperlipidemia is associated with skeletal muscle pathology, 10 male patients and 15 normolipidemic controls underwent a 45-minute standardized bicycle ergometer test at a load of 2 W/kg lean body mass (parallel study). One- and 8-hour postexercise increments in the plasma level of the muscle proteins creatine kinase (CK), myoglobin (Mb), and fatty acid-binding protein (FABP) were assessed as parameters for (subclinical) skeletal muscle pathology. The 8-hour postexercise increments in CK and Mb and 1-hour postexercise increment in Mb were significantly higher in patients than in controls, thus indicating increased exercise-induced muscle membrane permeability in combined hyperlipidemia. To investigate the effects of lipid-lowering intervention on skeletal muscle in combined hyperlipidemia, 21 subjects with combined hyperlipidemia were randomized double-blindly to receive 6 weeks of treatment with fluvastatin 40 mg/d, gemfibrozil 600 mg twice daily, or combination therapy. All subjects underwent an ergometer test before and after treatment. Gemfibrozil treatment alone reduced the CK increments 8 hours postexercise by 47% and the FABP increments 1 and 8 hours postexercise by 83% and 101%, respectively (all P < .05). Combined treatment reduced Mb increments 1 hour postexercise by 54% and FABP increments 8 hours postexercise by 44% (all P < .05). A highly significant correlation existed between therapy-induced changes in plasma triglycerides and changes in postexercise increments of FABP and Mb. In conclusion, combined hyperlipidemia is associated with an increased exercise-induced release of muscle proteins, which is ameliorated by triglyceride-lowering intervention. As FABP is an indicator for ischemia-induced skeletal muscle pathology, a possible explanation is the impaired muscle blood flow during hypertriglyceridemia, which may be reversed by triglyceride-lowering intervention. The mechanism and clinical relevance of these findings remain to be investigated.
Gemfibrozil is an effective drug in the treatment of hypertriglyceridemia and its effects on morbidity and mortality seem out of proportion to its lipid lowering actions. There is considerable interest in its potential effects on lipoprotein fatty acid composition and consequent effect on oxidative susceptibility. Experimental results are not conclusive regarding whether gemfibrozil alters lipid composition or oxidative susceptibility of lipoproteins in humans. Here we investigate this question using different methodology than employed in previous investigations.
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Clinicians must be aware of drugs metabolized via cytochrome P450 isoenzymes and identify those requiring risk-versus-benefit analysis before prescribing. Patients need to be educated as to signs and symptoms requiring immediate physician intervention.
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This study was undertaken to investigate the role of primary substrate composition and concentration on the attenuation of biodegradable emerging trace organic chemicals (TOrCs) in simulated managed aquifer recharge (MAR) systems. Four sets of soil columns were established in the laboratory, each receiving synthetic feed solutions comprising different ratios and concentrations of peptone-yeast and humic acid as the primary substrate to investigate the effect on removal of six TOrCs (atenolol, caffeine, diclofenac, gemfibrozil, primidone, and trimethoprim). Based on abiotic control experiments, adsorption was not identified as a significant attenuation mechanism for primidone, gemfibrozil and diclofenac. Caffeine, atenolol and trimethoprim displayed initial adsorptive losses, however, adsorption coefficients derived from batch tests confirmed that adsorption was limited and in the long-term experiment, biodegradation was the dominant attenuation process. Within a travel time of 16 h, caffeine - an easily degradable compound exhibited removal exceeding 75% regardless of composition or concentration of the primary substrate. Primidone - a poorly degradable compound, showed no removal in any column regardless of the nature of the primary substrate. The composition and concentration of the primary substrate, however, had an effect on attenuation of moderately degradable TOrCs, such as atenolol, gemfibrozil and diclofenac, with the primary substrate composition seeming to have a larger impact on TOrC attenuation than its concentration. When the primary substrate consisted mainly of refractory substrate (humic acid), higher removal of the moderately degradable TOrCs was observed. The microbial communities in the columns receiving more refractory carbon, were noted to be more diverse and hence likely able to express a wider range of enzymes, which were more suitable for TOrC transformation. The effect of the primary substrate on microbial community composition, diversity and gene expression potential confirmed its influence on TOrC degradation.
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We obtained data on incident melanomas from 20 of 36 qualifying randomized controlled trials (12 statin trials and eight fibrate trials), with a total of 70,820 participants. A total of 127 melanomas occurred among the 39,426 participants in the statin trials (59 among the 19,872 statin group participants and 68 among the 19,554 control group participants). A total of 27 melanomas occurred among the 31,394 participants enrolled in the fibrate trials (seven among the 12,324 fibrate group participants and 20 among the 19,070 control group participants). Overall, incidence of melanoma was not statistically significantly associated with the use of either statins (OR = 0.87, 95% CI = 0.61 to 1.23) or fibrates (OR = 0.45, 95% CI = 0.20 to 1.01). In a subgroup analysis by drug, only lovastatin use (in one trial) was statistically significantly associated with lower incidence of melanoma (OR = 0.52, 95% CI = 0.27 to 0.99).
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Bezafibrate and fenofibrate do not affect the pharmacokinetics or pharmacodynamics of repaglinide.
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A case of elevated creatine phosphokinase (CPK) levels associated with linezolid therapy in a patient on chronic antihyperlipidemic therapy is presented.
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Exposure of HepG2 and Hep3B cells to gemfibrozil (40 micrograms/ml), a hypolipidemic drug, resulted in a 2-fold induction of apo AI mRNA and, a one-third reduction in apo B mRNA but had no significant effect on apo E mRNA levels. The hypothesis that the mechanism of action of gemfibrozil involved the cytochrome P-450 system was tested by using ketoconazole, a P-450 inhibitor, which blocks the formation of endogenous polar sterols. When the cells were treated with ketoconazole at a concentration of greater than or equal to 15 microM, the levels of apo AI, and apo B mRNAs decreased by 50% and 35%, respectively, compared to the basal level. No significant effect on apo E mRNA level was observed during ketoconazole treatment. The effects of gemfibrozil and ketoconazole on various apolipoprotein secretion were studied using pulse-chase experiments. It was observed that the selective alterations in the rates of apo AI and apo B production were occurring at the level of synthesis. This observation is consistent with the findings indicating a strong direct correlation between hepatic apolipoprotein mRNA concentration and secreted apolipoprotein levels. The induction of apo AI mRNA by gemfibrozil was not apparent when the cells were simultaneously treated with ketoconazole. However, the level of apo B mRNA was reduced further to less than 55% of the control level suggesting that there might be an additive effect of these two drugs on apo B synthesis.
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It was suggested that postprandial lipoproteins (PPLp) may play an important role in atherogenesis. We studied PPLp metabolism and its response to drugs in seven hypertriglyceridemic subjects, 23 men with isolated low HDL-C levels, and nine non-diabetic glucose intolerant subjects. Results were compared with those found in a group of 19 healthy normolipidemic individuals. We used the vitamin A-fat loading test which specifically labels PPLp with retinyl palmitate (RP). In the hypertriglyceridemics the areas under RP curves of the chylomicrons were 6.3-fold and those of non-chylomicrons 2.9-fold higher than in normals (P < 0.01). Gemfibrozil 1200 mg/day caused a dramatic decrease in chylomicrons 73% and nonchylomicrons 31%. In subjects with isolated low HDL-C, RP chylomicron curves were significantly higher than in normals (17.733+/-6.821 vs 13939+/-6217 microg/l per h, P < 0.005). Bezafibrate 400 mg/day reduced RP chylomicrons and nonchylomicron levels by 35% (P < 0.0001) in 15 responders with an increase in fasting HDL-C 35+/-3 to 40+/-22 mg/dl (P < 0.0001). No response was found in eight subjects. In the nine glucose intolerant subjects, metformin reduced postprandial insulin area under the curve from 389 to 245 mU/ml (P <0.01) chylomicron and nonchylomicron RP areas were 3.6- and 3-fold higher than in normals and were reduced by 56 and 32%, respectively. In conclusion gemfibrozil, bezafibrate and metformin were shown to be beneficial in the clearance of PPLp in hypertriglyceridemic patients, subjects with isolated low HDL-C levels and nondiabetic glucose intolerant subjects, respectively.
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Chronic renal failure may be a risk factor for rhabdomyolysis associated with fibrates. Although rhabdomyolysis usually occurred when fibrates were combined with statins, a well-known class of agents that potentially induce rhabdomyolysis, precautions against serious adverse effects should also be taken with fibrate monotherapy.
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To compare the effects of gemfibrozil and lovastatin in patients with hypercholesterolemia and increased lipoprotein(a) [Lp(a)] levels.
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